The blood flow and penetration in the circulatory system of a living subject is dependent on the arteriole muscular tension, so-called tonus. A high tonus reduces the arteriole diameter and as a result the blood flow is reduced. The driving force of the flow is the aortic blood pressure. The elasticity of the aorta maintains the blood flow between heart contractions. Variations in the aortic pressure have a limited, secondary effect on the blood flow.
The tension of the arteriole muscles is released by an epidermal releasing factor (EDRF), in practice NO-gas, which is emitted by the arteriole inner epidermal tissue. The emission of EDRF is inhibited by hemoglobin. The arteriole muscular tension is asserted by neural system controlled demand. For local control this tension is released by EDRF and the release of EDRF is in its turn inhibited by the blood flow, as mentioned above. By the combined action of EDRF and the blood flow the blood distribution to different parts of the body of a living subject is controlled and it is possible to compensate for local pressure differences, lumen diameters etc.
With the tonus unchanged, an increased heart rate will not result in a significant increase of the blood flow. On the other hand, a decrease in tonus will increase the blood flow, and then the aortic pressure will fall, if the heart rate does not increase at the same time. An increased heart rate is normally controlled by the sinus node and catecholamine hormones. The sinus node controls the over all rate and the catecholamine hormones the propagation speed and contractibility of the heart muscle cells. The onset of both the sinus node control and the catecholamine hormones control is controlled by the autonomous nerve system.
In summary, the blood flow is controlled by the tonus, the driving force for the flow is the blood pressure in the elastic aorta, and the pressure in the aorta is maintained by the pumping action of the heart. During the pumping, the pressure in the left ventricle of the heart is equal to the aortic pressure as long as the aortic valve is open, the systolic phase. The right and left ventricles are parts of two systems, connected in series via the pulmonary system. From each ventricle the same volume of blood is pumped, however, at different pressures. The pressure in the left ventricle is approximately seven times higher than in the right ventricle. The same muscle is producing the pumping force, but the wall of the left ventricle is thicker than the wall of the right ventricle, see FIG. 1, which illustrates the pressures in the left ventricle P.sub.LV and in the right ventricle P.sub.RV as well as the aortic pressure P.sub.aorta as a function of time.
After closing the aortic valve the aortic pressure is exponentially decaying, the decay time being related to the peripheral resistance of the circulatory system or tonus. For a higher workload the blood flow increases and the aortic pressure P.sub.aorta decays more rapidly, see FIG. 2, which is a diagram analogous to that in FIG. 1.
If the delivery of stimulation pulses is triggered by a given minimum aortic pressure level the stimulation rate will be increased in response in response to an increased workload, so-called rate response stimulation. If the stimulus is moved to an earlier timing position, the systolic pressure will start from a higher starting pressure and hence a higher end systolic pressure should result. However, this is not the case if the heart is ischemic. The pumping of the heart is then less effective and the blood volume output per heartbeat is less and no pressure increase will result.
For the pumping action the heart needs energy in the form of oxygen and glucose. About 60% of the oxygen in the heart interstitial fluid is consumed within one heartbeat. If the energy supply to the heart is disturbed the heart contractability and the pumping action of the heart are severely deteriorated and an oxygen shortage or ischemic situation will rapidly develop.
Ischemia results from insufficient blood flow through the heart muscle. The reason therefor is blocking or passage congestion of coronary blood vessels of the heart. There are three categories of ischemic deceases, viz. angina pectoris, heart infarction and heart insufficiency and an ischemia is experienced by the patient as a severe chest pain.
During systole when the aortic valve is open, no blood can flow to the heart muscle. The pressure inside the heart is substantially equal to the aortic blood pressure. After closure of the aortic valve, some time is needed for the oxygen delivery to the heart muscle such that contractability is regained. In case of coronary blood vessel congestion this time is considerably increased. It is known that the developement of an ischemia accelerates with increasing heart rate, i.e. increasing workload. In a pacemaker system with a stimulation rate that increases with increasing workload, ischemia is a major limitation for the rate increase. As blood penetration of the heart muscle is possible only during diastole, when the aortic pressure is higher than the ventricular pressure, a rate increase, which results in a reduction of the diastolic period, will severe the ischemic situation, cf. FIG. 2. As mentioned above, in a deceased heart the normal rate control by the sinus node is lost. A pacemaker is therefore needed to maintain a proper heart rate and different systems are used to adjust the stimulation rate to increased demands, associated with e.g. increased workload. The ischemic effect can be especially serious for patients having such rate response pacemakers.
A method and apparatus for detecting myocardial ischemia is described in U.S. Pat. No. 4,821,735. The systemic vascular resistance (SVR) in a subject is then monitored and the presence of myocardial ischemia is detected when the SVR increases by at least 60% over a base line value, said SVR being defined as the ratio between the arterial pressure P and the peak dP/dt at the time of the peak of the dP/dt.
A device for analyzing the function of a heart is described in U.S. Pat. No. 5,427,112. A heart variable is then measured and a parameter signal related to the heart variable is generated, whereupon the heart variable is plotted against the parameter signal to obtain a curve. By analyzing the morphology and chronological course of the curve functional aberrations of the heart, such as bradycardia, tachyarrhythmia, ischemia etc., can be detected.
In U.S. Pat. No. 5,497,780 an apparatus is described for determining an ischemia by measurements of electric potentials between at least three implanted measuring electrodes, two of said electrodes being implanted with their poles in the heart and the third electrode being implanted with its pole lying outside the heart.
In U.S. Pat. No. 5,476,484 an apparatus is disclosed for determining the peripheral resistance to flow in a living subject by measuring changes in the pressure drop in an artery during diastole for determining the physical condition of the subject, like state of health or workload (activity level). A rate-responsive heart stimulator is then controlled dependent on this peripheral resistance.
The purpose of the present invention is to provide a new reliable ischemia detector, which can be used also for eliminating the above discussed problems for ischemic patients carrying a heart stimulator.